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Pharm 2 > Midterm > Flashcards

Midterm Flashcards

1
Q

Dose of fentanyl

A

5-10 mcg/kg (50-100 mcg clinical)

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2
Q

Dose of propofol

A

1-2 mg/kg

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3
Q

Dose of etomidate

A

0.2-0.3 mg/kg

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4
Q

Dose of Versed

A

0.1-0.2 mg/kg (1-2 mg clinical)

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5
Q

ketamine dose

A

2-4 mg/kg (10-50 mg clinical)

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6
Q

What stage of awareness is a MAC case?

A

3- subconscious, implicit recall

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7
Q

What stage of awareness is a general anesthesia case?

A

4- no awareness or recall

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8
Q

MoA of inhalational agents

A

activate GABA and glycine, inhibit glutamate

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9
Q

What is MAC?

A

minimum alveolar concentration- concentration required to keep 50% of humans from moving in response to painful stim

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10
Q

VP of halothane

A

244

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11
Q

VP of isoflurane

A

240

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12
Q

VP of desflurane

A

669

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13
Q

VP of sevoflurane

A

170

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14
Q

BG coefficient of nitrous

A

0.46

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15
Q

BG coefficient of halothane

A

2.54

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16
Q

BG coefficient of isoflurane

A

1.46

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17
Q

BG coefficient of desflurane

A

0.42

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18
Q

BG coefficient of sevoflurane

A

0.69

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19
Q

MAC of nitrous oxide

A

104

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20
Q

MAC of halothane

A

0.75

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21
Q

MAC of isoflurane

A

1.2

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22
Q

MAC of desflurane

A

6

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23
Q

MAC of sevoflurane

A

2

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24
Q

OG coefficient of nitrous

A

1.4

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25
Q

OG coefficient of halothane

A

224

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26
Q

OG coefficient of isoflurane

A

98

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27
Q

OG coefficient of desflurane

A

18.7

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28
Q

OG coefficient of sevoflurane

A

55

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29
Q

What conditions increase MAC?

A

youth, hyperthermia, hypernatremia, chronic ETOH, stimulants

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30
Q

What conditions decrease MAC?

A

age, hypothermia, pregnancy, acute ETOH intox, other anesthetics, drugs (benzos, opioids, alpha 2 agonists)

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31
Q

MAC awake

A

50% respond to verbal stim- 0.2-0.3

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32
Q

MAC bar

A

block autonomic reflex- 1.7-2x MAC

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33
Q

MAC intubation

A

2x MAC

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34
Q

ED95

A

level where 50% don’t respond- 1.3x MAC

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35
Q

Fick’s law of diffusion

A

rate of diffusion directly proportional to gradient, surface area, and diffusion coefficient, and inversely proportional to membrane thickness

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36
Q

Graham’s law

A

rate of effusion inversely proportional to square root of molecular weight

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37
Q

Blood gas coefficient

A

indicates how fast drug gets to site of action

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38
Q

Oil gas coefficient

A

indicates potency

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39
Q

What does increased CO do to uptake?

A

uptake increases and induction is slower

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40
Q

What gas is metabolized the most?

A

halothane

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41
Q

Where is nitrous metabolized?

A

in the gut by aerobic bacteria

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42
Q

What two gases are structurally similar?

A

iso and des- differ only by Cl atom

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43
Q

Which gas metabolite is a concern for liver?

A

halothane- hepatitis

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44
Q

Which gases have the least effect on blunting autoregulation?

A

isoflurane or desflurane

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45
Q

Who do you avoid using halothane in?

A

cardiac defects (down’s syndrome)

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46
Q

What gas can cause bradycardia and junctional rhythms at high MAC?

A

sevo

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47
Q

What gases at higher doses will exhibit sympathetic response?

A

desflurane and isoflurane

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48
Q

Which gases produce the most “coronary steal”?

A

iso and des (sevo the least- can use to precondition)

49
Q

What condition should you avoid the use of nitrous oxide with?

A

pulmonary hypertension

50
Q

Describe gas breathing

A

increased RR, decreased TV

51
Q

What metabolite is toxic to kidneys?

A

Compound A from sevo (avoid in renal patients if you can)

52
Q

How do you reduce production of compound A?

A

higher flows, keep soda lime fresh, use lower concentration

53
Q

How do anesthetic gases decrease total hepatic blood flow?

A

decrease portal vein flow

54
Q

Complication of N2O use?

A

reduced immune function- disrupts DNA synthesis by inactivating B12

55
Q

Contraindication to nitrous?

A

air containing cavities (air embolus, closed pneumo, etc)

56
Q

What is the mechanism of malignant hyperthermia?

A

activation of ryanodine receptors- increased release of calcium from SR–> sustained m. contraction–> increased metabolism= heat production

57
Q

What are the signs and symptoms of MH?

A

tachycardia, hypercarbia, hyperthermia, masseter spasm, tachypnea, arrhythmias, metabolic acidosis, m. rigidity, myoglobinemia, hyperkalemia

58
Q

Treatment for MH

A

dantrolene, stop agents, 100% O2 with charcoal filter, arterial access, cooling measures

59
Q

What does dantrolene do and what are the considerations?

A

blocks coupled calcium entry- causes m. relaxation so may need respiratory support

60
Q

Which opioid receptor has antishivering effects?

A

kappa

61
Q

Order of opioid potency from least to greatest

A

demerol < morphine < dilaudid < alfentanil < fentanyl < remifentanil < sufentanil

62
Q

Which opioids have the fastest onset?

A

fentanyl, sufentanil, remifentanil

63
Q

Which opioid has the shortest duration of action?

A

sufentanil (and fentanyl)

64
Q

What causes cardiovascular effects from opioids?

A

histamine release (naturally occurring opioids)- venodilation, bradycardia–> hypotension

65
Q

What can occur with high doses of synthetic opioids?

A

muscle rigidity- decreased chest wall compliance

66
Q

What is the longest acting opioid?

A

morphine

67
Q

Where is morphine metabolized and what is it conjugated to?

A

liver- morphine 3 (inactive- seizures), morphine 6 (active- resp depression)

68
Q

Is morphine more for dull or sharp pain?

A

dull

69
Q

Describe codeine

A

natural occurring opioid, 10% breaks down to morphine, more used for anti-tussive properties than pain

70
Q

Why would you use Dilaudid over morphine?

A

renal insufficiency- no active metabolites

71
Q

Dose of Dilaudid

A

0.2-0.5 mg IV

72
Q

What is demerol used for?

A

post-op shivering

73
Q

When should you avoid demerol?

A

renal insufficiency (active metabolite buildup –> seizures), and concurrent use with MAOIs (serotonin syndrome)

74
Q

Storage site of inactive fentanyl metabolites?

A

lungs- significant first pass pulmonary uptake

75
Q

How is remifentanil metabolized?

A

esterases in blood (majority) and some by N-dealkylation

76
Q

What can remifentanil boluses cause?

A

bradycardia unresponsive to vagolytics- may need epi

77
Q

Rare effect of remifentanil?

A

hyperalgesia

78
Q

What opioid is best for chronic pain?

A

methadone

79
Q

Why is fentanyl preferred over alfentanil?

A

longer duration of action

80
Q

What opioid is preferred for cardiac and airway cases?

A

sufentanil- significant analgesia

81
Q

Considerations for using opioids in neuraxial analgesia

A

smaller doses, watch for respiratory depression, must be preservative free

82
Q

What is the ceiling effect in regards to agonist-antagonists?

A

increased doses do not produce additional responses

83
Q

How do you administer Narcan?

A

20-40 mcg IV carefully titrated to prevent rapid reversal (can cause sympathetic response, pulmonary edema, severe pain, arrhythmias)

84
Q

Duration of Narcan?

A

1-4 hours

85
Q

When should you avoid using toradol?

A

renal patients, asthma patients, and ortho (inhibits bone healing)

86
Q

What stage is a patient at risk for laryngospasm?

A

stage 2

87
Q

CV effects of propofol?

A

tachycardia on induction, decreased SVR, hypotension

88
Q

Propofol Infusion Syndrome symptoms

A

acidosis, hypertriglyceridemia, renal failure, bradycardia, hypotension, rhabdo

89
Q

What are some phenomena that may occur on induction with propofol?

A

twitching, opisthotonus

90
Q

What is a common side effect of etomidate?

A

myoclonus

91
Q

Does a standard induction dose of etomidate cause apnea?

A

no

92
Q

What do you want to ensure before giving barbituates?

A

adequate volume status (can cause profound vasodilation)

93
Q

What can barbituates trigger?

A

acute intermittent porphyria

94
Q

How is ketamine different from other induction drugs?

A

sympathomimetic (increased HR, BP, CO), increases ICP, CMRO2; also a NMDA antagonist instead of acting on GABA

95
Q

What population is ketamine good for?

A

severe asthmatics

96
Q

What may ketamine cause?

A

increased salivation

97
Q

List benzos in order of shortest to longest half life

A

versed (2 hours), Ativan (15 hours), valium (30 hours)

98
Q

Schedule 1 drugs

A

heroin, LSD, marijuana, qualudes, ecstasy

99
Q

Schedule 2 drugs

A

cocaine, meth, pentobarb, fentanyl, codeine

100
Q

Schedule 3 drugs

A

barbituates, hydrocodone, ketamine

101
Q

Schedule 4 drugs

A

phenobarb, valium, butorphanol

102
Q

Schedule 5 drugs

A

buprenorphine, codeine cough syrup

103
Q

What are the different “tropys”?

A

ino- force of contraction; chrono- rate; dromo- speed of electrical conduction; lusi- relaxation

104
Q

How do beta blockers work?

A

slow phase 4 depolarization

105
Q

What are the vascular effects of nitric oxide?

A

vasodilation, antithrombotic, anti-inflammatory, anti-proliferative

106
Q

What are drugs that act on the nitric oxide pathway?

A

hydralazine (arterial), nitro (venous), nitroprusside (both)

107
Q

What is a neuro consequence of using nitro or nitroprusside?

A

increases ICP

108
Q

What is a possible complication of nitroprusside?

A

cyanide toxicity

109
Q

What are the effects of CCBs?

A

varying degrees of myocardial depression, vasodilation, activation of ANS

110
Q

What do ACEIs do?

A

reduce BP by blocking the conversion of angiotensin I to angiotensin II

111
Q

What do ARBs do?

A

reduce BP by blocking angiotensin II receptors

112
Q

What are some interactions of CCBs with anesthetics?

A

potentiate m. relaxants and local anesthetics

113
Q

How do you treat refractory hypotension as a result fo ACEIs?

A

vasopressin or methylene blue

114
Q

What are the 4 classes of antidysrythmics?

A

1- sodium blockers; 2- beta blockers; 3- K blockers; 4- Ca blockers

115
Q

What is the effect of lidocaine on the heart?

A

blocks fast Na channels, decreases automaticity, accelerates repolarization

116
Q

What kind of beta blockers do we prefer to use?

A

selective- like esmolol

117
Q

What is amio?

A

K channel blocker- used for life threatening ventricular rhythms

118
Q

What kind of CCB is good for neuro cases?

A

nimodopine (crosses BBB)

Pharm 2 (7 decks)

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